Interferon-alpha and then interferon-beta-1b were first used in MS studies because of their known antiviral properties. At the present time, however, there is no accepted evidence that acute or chronic viral infection itself has any role in the causation of MS attacks or progression. There have been numerous studies of what the interferons do in the human body and specifically how they affect mechanisms of tissue damage in MS. A number of effects that both interferons possess should have a favorable effect in MS.
Among other properties, interferons decrease the activation (turning on) of lymphocytes and macrophages in a number of different ways. Another effect is to decrease the ability of activated cells to stick to the inside of the blood vessels of the brain and spinal cord via adhesion molecules. The interferons also interfere with cells already stuck to the inside of the blood vessels and their ability to initiate the series of events that allow the cells to eat a hole through the blood vessel's wall. This is accomplished through a number of different mechanisms, including the inhibition of metallo-proteases (MMPs). It is generally accepted that these several mechanisms are important in the benefits of Betaseron, Avonex, and Rebif in MS.
Glatiramer acetate (Copaxone), although not an interferon, appears to behave as theorized. As designed, it seems to function as a decoy for the immune system. It prevents myelin-like proteins from activating mechanisms causing additional myelin damage. Extrapolating from animal studies, there appear to be a number of beneficial effects on immune function when using Copaxone. There is recent evidence that Copaxone plays an important role in MS by switching off cyto-toxic lymphocytes (CD8+ cells) and turning on immunosuppressive activity.
members of a group of secreted neutral proteases that degrade the collagens of the extracellular matrix. Members of this group are important in maintaining and breaching the integrity of the blood-brain barrier.
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